Generally, coagulation (i.e., thrombogenesis) is the process by which blood changes from being flowable to forming clots. Coagulation is an important part of hemostasis, which is the cessation of blood loss from a damaged vessel, wherein a damaged blood vessel wall is covered by a platelet and fibrin-containing clot to stop bleeding and begin repair of the damaged vessel. Disorders of coagulation can lead to an increased risk of bleeding (hemorrhage) or obstructive clotting (thrombosis). Coagulation is highly conserved throughout biology; in all mammals, coagulation involves both a cellular (platelet) and a protein (coagulation factor) component. Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the vessel. Blood begins to coagulate upon exposure to air. Also, exposure of the blood to proteins, such as tissue factor, initiates changes to blood platelets and the plasma protein fibrinogen, a clotting factor. Platelets immediately begin to form a plug at the site of injury, which is called primary hemostasis. Secondary hemostasis occurs simultaneously where proteins in the blood plasma, called coagulation factors or clotting factors, respond in a complex cascade to form fibrin strands, which thicken the blood strengthen the platelet plug.
It is apparent that the balance between flowable blood and coagulating blood is tenuous. As such, tipping the balance from flowable blood to coagulating blood can be beneficial in a number of instances. For example, when a blood vessel becomes compromised so that there is an opening allowing blood to escape, the body signals for the initiation of the events to coagulate the blood and repair the vessel. Therefore, it can be advantageous to have systems and methods that promote blood coagulation. However, it is difficult to determine which pathway can be inhibited for promoting effective blood coagulation in particular circumstances.